Bipolar Affective Disorder (BPAD) - Clinical Case Series #2
Adapted by Prof. Henry O'Connell from his book "Evolution and Psychiatry: Clinical Cases" - Edited by Dr Gurjot Brar
Welcome to the second of our clinical case series, exploring common mental disorders through the lens of evolutionary psychiatry. A ‘problem-based learning’ (PBL) approach is taken with learning outcomes defined at the outset, followed by several clinical encounters with fictional scenarios, interspersed with theory responding to the learning objectives. This method has emerged globally in medical curricula and has a good evidence base in medical education promoting self-directed learning. We hope you enjoy this format and look forward to your feedback.
This case series will often refer to key principles defined in the following article published in July 2023 which serves as a primer:
Evolution – basic principles & applications to health and illness
"Evolution and Psychiatry: Clinical Cases" is available hereThanks for reading Evolution and Psychiatry! Subscribe for free to receive new posts and support my work.
Bipolar Affective Disorder (BPAD)
Learning Objectives
1. Outline briefly the key facts about BPAD relating to clinical features and diagnostic criteria, epidemiology, aetiology, pathophysiology and management
2. Describe the potential adaptive benefits of normal mood variation
3. Describe the principle of Viewing Diseases as Adaptations (VDAA) and how this is important in how we conceptualize conditions such as BPAD
4. Outline how the evolutionary perspective can help inform treatment strategies for BPAD
5. Describe how evolutionary principles can be used in psychoeducation with families affected by BPAD
6. Outline how the evolutionary perspective can help inform research strategies for BPAD
Clinical station 1: ‘he’s been a bit of a handful’
You are the Consultant Psychiatrist in charge of a busy acute psychiatric inpatient unit in an Irish city hospital. You return from a long weekend off work and start your Monday morning rounds with a junior doctor (i.e. Non-Consultant Hospital Doctor or NCHD) and Staff Nurse.
‘It was a pretty quiet weekend, doc’, says the nurse. ‘We’ve had just the one new admission. But he’s been a bit of a handful. Denis Hennessy is his name. He’s aged 22, a recent college graduate in creative writing and from a farming background. He was in Australia for the summer after finishing college, working in bars, and just returned last week. It looks like he had some sort of breakdown over there just 3 or 4 weeks ago but somehow managed to make it home to Ireland with the help of a friend. He’s been all over the place since getting back. He hasn’t been sleeping, he’s been uncharacteristically irritable with family and making big plans to sell his father’s farm and build some type of mega-church from where he can preach. He started to become hostile towards his parents on Saturday when they wouldn’t go along with his plans and he was brought in by our Assisted Admissions team. He is involuntary, signed in under the Mental Health Act.’
You look to the NCHD and ask for her input.
‘Yes Dr. Walsh, just as the Nurse has said. Also, he seems to have been partying for several weeks in Australia directly before coming home. He was drinking large quantities of alcohol daily, smoking a lot of marijuana and he had a fall. We have checked him out physically and did neuroimaging, which was normal. He is challenging and taking medication only with close supervision. He has zero insight into his condition – he thinks we just don’t want him preaching the truth, to use his term. Oh and one more observation – he’s actually quite hilarious. He makes everyone laugh, even though that isn’t always his intention’.
You note the clinical entries from the weekend and agree with colleagues who have already assessed him that this appears to be a manic episode with psychotic features, apparently his first experience of mental illness. Your meeting with Denis confirms this. He greets you with:
‘Well here’s the little man who’s going to let me go free. About time too – it’s nearly 9 o’clock. Clippity clop, nine o’clock, you’re the doc, but you’re not Dr. Spoc’.
He is disheveled, disinhibited, emotionally labile, pressured and tangential in his speech and, as the NCHD has observed, unintentionally hilarious.
Later in the day you receive a telephone call from Denis’s mother. She is very upset, shaken by his recent behaviour and she wants to know how he is doing and what is actually ‘wrong’ with him. She tells you this is like a flashback to her childhood, when her own mother was frequently admitted to a local psychiatric hospital. She thinks her grandmother may have had similar problems.
Learning Objective 1:
Outline briefly the key facts about BPAD relating to clinical features and diagnostic criteria, epidemiology, aetiology, pathophysiology and management
BPAD is a major psychiatric disorder characterized by extreme and sustained mood variations, often with psychotic symptoms in the acute phase, and associated with significant behavioural disturbance and dysfunction. In BPAD I, the main focus for this case, there are discrete episodes generally of several weeks duration of significant depression and, less often, mania or mixed affective states.
Related disorders include BPAD II, in which the upswings in mood are hypomanic in that they do not cause significant functional impairment, while cyclothymic disorder involves lifelong mood variation where the episodes are not severe enough to constitute depressive or manic episodes. Furthermore, up to one third of people diagnosed with Recurrent Depressive Disorder (RDD) may have had hypomanic episodes, suggesting a continuum of mood disorder phenotypes, with frequent comorbid alcohol and substance use disorders. Important differentials include Schizophrenia (distinction may be difficult in the acute phase and only clarified over prolonged assessment) and Borderline Personality Disorder, where the mood changes are more fleeting, often arising in the context of interpersonal difficulties.
Regarding BPAD type I, onset is usually in the early 20s, males and females tend to be equally affected and lifetime prevalence is approximately 1%. As with all major psychiatric disorders, multiple genes are implicated and it is now recognised that there is more genetic overlap with Schizophrenia and Schizoaffective Disorder than was previously thought to be the case.
Close family members carry a substantially increased risk of other mood and perhaps even substance use disorders, so that similar genotypes can be conceptualized as having different phenotypic manifestations.
Dopaminergic overdrive is a key mediator in the manic phase, hence the role of antipsychotic medications. Longer term prophylaxis is best achieved with Lithium and/or anticonvulsant mood stabilizers such as Valproate and Carbamazepine. As a general rule, functional level between episodes tends to be relatively good in comparison to Schizophrenia but, for BPAD type I at least, lifelong maintenance medication is the norm.
Clinical station 2: ‘Doctor – I have some other questions’
It is now three weeks since Denis was admitted to hospital. He has had a good clinical response to a combination of Lithium, Olanzapine and Lorazepam. His mood has returned to baseline, he is sleeping well and his behaviour is appropriate and cooperative. He accepts that he was ‘not himself’ prior to admission and that he needs to continue with medication for the next several months at least. He is ready for discharge and keen to get home, although he is anxious about meeting his parents as he is embarrassed and remorseful about events before admission.
He has told you in recent days that he remembers arguing especially intensely with his father prior to being brought to hospital.
‘You see, Dad always expected me to take over the family farm, being the only son. He couldn’t imagine how a man would ever want to be a writer or journalist. He used to make snide comments about my career choice and suggest I was ‘soft’ and he told me once that I was letting the Hennessy name down, that the farm would have to be sold and the land would leave the family for the first time in five generations. I soaked up his comments for years and said nothing, but I was having none of it when I got back from Australia. I told him that I wasn’t going to be a foolish slave to his cows for the rest of my life, that I had bigger plans. And then I told him about the mega-church idea. It’s so embarrassing now even telling you. I’m going to find it hard to face him and the rest of the family again’.
You meet with Denis on the day of his discharge to clarify his follow-up plan. It turns out that he has actually had two previous depressive episodes, treated with antidepressants by his Family Doctor, and his alcohol and drug use in Australia seems to be have been secondary to his elated mood, so you are satisfied that you now have enough information to make a diagnosis of BPAD type I. Denis has already had detailed psychoeducation with the NCHD and nursing staff, he has learned a lot about BPAD and he agrees that his symptom profile is consistent with the diagnosis.
As you write his prescription and give him an outpatient clinic date, he stops you and says:
‘Doctor – I have some other questions. I’ve been thinking a lot about mood changes and bipolar illness. Isn’t mood change normal for people? I’ve noticed over the years that I get surges of energy when I can do loads, like when I was doing exams or projects in college. And then I might have down times, but I could rest and reflect then. I didn’t always need to see a doctor for these changes. I know this medication has helped, but now I’m worried that it will take away my normal emotions and drive. If I become a writer or journalist then the work is going to be unpredictable. I can see myself working intensely for a few months and then having fallow periods when I will need to slow down. Is there a chance the medication might make my moods too ‘even’ for that type of lifestyle? And isn’t it true that lots of really creative and productive people are actually bipolar?’
Learning Objective 2:
Describe the adaptive benefits of normal mood variation
Randolph Nesse (2018) makes clear the dramatic (but sometimes ignored) distinction between everyday ‘low mood’ in contrast to clinical level depression with its pervasively depressed mood and associated biological features such as diminished energy levels, anhedonia, disturbed sleep, appetite changes and suicidal thinking.
The universal capacity for normal mood variation suggests potential adaptive benefits. Mildly depressed mood has been demonstrated to be associated with more objective appraisals of the world, specific situations and of ourselves. It seems intuitive then that, when confronted with difficult or challenging situations that the capacity for slowing down and becoming more objectively analytical, reserved and discerning is likely to lead to better outcomes. At a more primitive level, adopting the depressed state may have benefits in terms of conflict avoidance with more powerful foes and may help in eliciting care and support from peers. These issues will be discussed in more detail in the case on depression.
And just as low mood (like all emotional states) is context dependent and may be adaptive in certain situations, likewise opportunities (and, sometimes, threats) may elicit brief bursts of elevated mood, energy upsurges, reduced need for sleep and overly optimistic thinking.
The evolutionary perspective suggests that BPAD (type I at least) can be conceptualized as a pathological and dysfunctional extreme of these normal mood variation capacities. Randolph Nesse uses the analogy of the ‘moodostat’ here, i.e. the normal internal corrective mechanisms for preventing our mood from going too low (clinical level depression) or too high (elated or mixed affective states) is somehow faulty in those with BPAD, with mood levels under and overshooting the mark and changes often occurring without any significant external stimulus or stressor.
Mania has been described as ‘an unconstrained acquisitive drive which is activated by evolutionary ancient systems involved in the regulation of arousal and ambition’ (Wilson, 1998).
Learning Objective 3:
Describe the principle of Viewing Diseases as Adaptations (VDAA) and how this is important in how we conceptualize conditions such as BPAD
One of the most serious traps of a misguided evolutionary perspective is to view all mental states and disorders as being potentially useful and adaptive. As any clinician knows from treating people in the acute phases of BPAD especially, the extremes of mood, frequent accompanying psychotic symptoms and associated behavioural dysfunction are clearly not adaptive and are unlikely to have ever served a useful purpose at any stage of our evolutionary history. In fact, we know that mania carried with it a mortality rate of approximately 25% (due to e.g. exhaustion and death by misadventure) in the days before effective psychotropic medication was available.
Therefore, the universal capacity for normal mood variation and even the relatively mild mood changes seen in Cyclothymic Disorder or BPAD II can be conceptualised as being potentially useful (albeit often unpleasant for the individual) in facilitating short term immersion in or indeed avoidance of important challenges, threats and opportunities. In stark contrast, the ‘moodostat’ issues of BPAD I are far from helpful, especially in the acute phases.
This knowledge and perspective is important and useful when confronted with questions from patients and families about the potential for creativity and productivity in BPAD I and concerns about dampening potential with mood stabilizer medication. Such ideas can be used to rationalise lack of cooperation with medication and psychotherapy support. In fact, it should be argued that compliance with a comprehensive medication and psychotherapy plan is likely to reduce the frequency and severity of relapses, thus reducing the loss of social capital associated with major mental illness and ultimately optimising the individual’s quality of life, functional level, creativity and productivity in the longer term.
Learning Objective 4:
Outline how the evolutionary perspective can help inform treatment strategies for BPAD
A comprehensive and sustainable individual treatment plan must have as its foundation a multifaceted assessment. As outlined earlier, the history of depressive episodes and at least one manic episode is needed for a diagnosis of BPAD I. Similarities in the acute phase between BPAD and psychotic disorders such as Schizophrenia means that longitudinal assessment is necessary and helpful in clarifying diagnosis.
In addition to this traditional approach to clarifying diagnosis, the SOCIAL review of systems outlined by Nesse (2018) adds further quality to the assessment and helps inform a bespoke treatment plan for individual patients. Thus resources relating to Social (friends, groups, social influence, etc.), Occupation, Children and family, Income, Abilities and other personal resources and Love and sex should be considered in how they colour the current presentation and in their importance for future prognosis. Deficits or challenges in specific areas should be addressed through targeted psychosocial interventions and supports.
As outlined in Learning Objective 3 above, the importance of maintenance medication should always be stressed and any misguided ideas about dampening creativity or productivity should be addressed.
The risk of adopting a self-destructive ‘fast life history strategy’ (see the previous clinical case on ADHD) in chronically undertreated BPAD, with all its attendant consequences, should also be outlined to patients and families and serve as a powerful motivator for psychoeducation and optimizing compliance with all available treatment options.
One of the most powerful aspects of the evolutionary perspective in the treatment of mental disorders are the many explanatory models provided by this approach. Thus concepts such as the role of emotions in everyday life, normal mood variation and the ‘moodostat’ may help convey meaning to patients, thus improving their likelihood of acceptance of the condition and improving their likelihood of compliance with necessary treatment. This psychoeducational impact alone has the potential for helping countless patients and their families and saving them from lost years and potential that may otherwise occur due to diminished insight and understanding regarding this potentially devastating mental disorder.
Clinical station 3: ‘I’m his sister – they say I’m the arty one’
It is now three months since Denis was discharged from hospital. He has done well, continuing with medication, attending your clinic for regular follow-up and he has started work as a journalist with a local newspaper. He plans to write a series of articles about his experience of mental illness as he feels this will help destigmatize BPAD and also help him process what happened. He calls your clinic to ask if you will meet with Carol, one of his sisters. She has some questions about BPAD and he is fine with you meeting her.
Carol attends your clinic the following week. She is stylishly dressed, wearing brightly coloured clothes, strong perfume and with a purple scarf in her hair. You notice that she is pregnant, possibly into the second trimester. When she enters your office she looks at you intensely, grasps your hand and says:
‘You know my brother, Denis Hennessy. I’m his sister – they say I’m the arty one’.
Carol is in her early thirties and works as a dance instructor and choreographer. She says she has been appointed as the ‘family spokesperson’ to ask questions on behalf of everyone. She asks you multiple questions about BPAD, in terms of symptoms and treatment (see Learning Objective 1). She says that, like Denis, she is a little dubious about the idea of medicating emotions, but you go through with her again some key principles relating to normal emotions and the dangers of Viewing Diseases as Adaptations (VDAA) (see Learning Objectives 2 and 3). She agrees with you on most of the points.
‘But I’m a little moody myself, Dr. Walsh. In fact, some of the best big decisions I’ve ever made were when I was on an upswing’, she smiles and points to her abdomen as she says this. ‘Unlike Denis, I’ve never needed medication. And I’m a few years older. But then we have two older other sisters who are not doing so well. Mary lives in Dublin and I know she’s an alcoholic. Everyone in the family knows it. But Mary doesn’t know it. I wonder sometimes if Bipolar is the root cause of her problems. And then there’s Jane, who is always miserable but will never get help. And of course there was our grandmother and great-grandmother on our mother’s side, but we don’t really know what was wrong with them, it’s so long ago. And now with my own baby on the way, I’m wondering if I’ve passed on the genes to him or her’.
Learning Objective 5:
Describe how evolutionary principles can be used in psychoeducation with families affected by BPAD
As outlined in earlier Learning Objectives, the risk of BPAD is significantly increased in close relatives. Therefore, the condition is strongly genetic, although multiple gene effects are at play. Review of the family tree of an individual with BPAD type I may reveal other family members with differing or less severe clinical phenotypes, such as in this case. In first-degree relatives of patients with bipolar disorder, there is evidence of the preservation of some genes predisposing to bipolar disorder which confer greater creativity, charism and leadership – all proxies for reproductive success (Wilson, 1998).
Family therapy and psychoeducation outlining shared genetic risk but with different phenotypic manifestations is likely to lead to a more collective and cooperative approach to supporting the most severely affected individuals.
Evolutionary interpretations of specific aspects of BPAD may also be helpful in individual and family oriented therapy. For example, mania can be conceptualized as a state whereby the individual exhibits a ‘pathological extreme of dominance behaviour’ (Brune, 2016), thus leading to reversal of usual asymmetries. In this case, while in the manic state Denis tried to turn the tables on his usually dominant father.
Finally in the family, understanding the role of mood and it’s variability can allow for clearer distinctions between normal mood variability when the patient is stable, compared with an imminent relapse, thereby reducing levels of expressed expression and stigma.
Learning Objective 6:
Outline how the evolutionary perspective can help inform research strategies for BPAD
Future research strategy on BPAD that is informed by an evolutionary perspective can be divided into research on ‘normal’ mood variation and on BPAD itself along with related disorders.
Research on normal mood variation should focus on the nature of triggers and contexts for certain emotional states (e.g. frustration in pursuit of a goal leading to apathy, loss leading to sadness), the mechanisms by which these emotional states are medicated (i.e. cognitive, neurophysiological, etc.) and the potential benefits of normal mood variation (e.g. the concept of ‘depressive realism’ or the need for relatively unbridled optimism in the face of significant challenges).
Research on BPAD and related disorders should focus on defining the mechanisms behind the normal ‘moodostat’ and identifying factors (cognitive, neurophysiological, endocrine, etc.) that cause this putative mechanism to become overly sensitive or faulty.
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It seems likely that ADHD characteristics are more problematic in modern societies than they were for our ancestors, but unlikely that they were ever "an adaptation" that gave net advantages. In the natural environment, individuals away from the mean of any continuous trait are generally expected to have lower than average fitness. If the trait is shaped by tradeoffs, those individuals would also be expected to have some advantages, despite net disadvantages. Looking for these tradeoffs is a productive approach to understanding the fitness effects of individual differences.
The diagnosis of 'schizophrenia' whether paranoid, disorganized , catatonic or otherwise says alot more about the psychiatrist than it does about the patient https://open.substack.com/pub/callystarforth/p/the-weapon-of-psychiatry?r=1eq51l&utm_campaign=post&utm_medium=web